Thyroid and Parathyroid Disease
Adam Michael Kravietz
Jessica L. Buicko
Although the Romans observed “goitres” among the peoples of the Alpine regions during their conquests, the term “thyroid,” Latin for “shield shaped,” dates to the 1500s.1
Parathyroid gland was identified by Ivar Sandström in 1880, but the role of the gland was not elucidated until the link between the gland and hypocalcemic tetany following thyroidectomy was made in the early 1900s by William MacCallum and William Halsted.2
Early thyroid and parathyroid surgery had high mortality rates due to air embolism, sepsis, asphyxiation, and hemorrhage.
Descriptions of recurrent laryngeal nerve (RLN) damage during surgery date back to the sixth century AD.
Improvements in antiseptic technique and anesthesia in the mid-1800s drastically reduced mortality.1,2
Kocher won the Nobel Prize in 1909 for his thyroidectomy surgery, and Lahey published his technique to dramatically reduce RLN palsies by ligating the inferior thyroid artery in 1938.1
RELEVANT ANATOMY
Thyroid gland begins developing at about week 4 of gestation, then descends from the base of the tongue to its final location inferior to the thyroid cartilage by the week 7 of gestation.
Thyroid gland begins producing thyroid hormone at about week 11.
The thyroid has 2 lateral lobes with a connecting isthmus across the midline, an anterior suspensory ligament tethering the gland to the thyroid and cricoid cartilages, and a posterior suspensory ligament tethering the gland to the cricoid cartilage and first 2 tracheal rings.
Covering the thyroid gland anteriorly are the sternohyoid and sternothyroid muscles.
Blood supply is received from the superior thyroid artery (branch of the external carotid) and the inferior thyroid artery (branch of the thyrocervical trunk).
Venous drainage is via the superior, middle, and inferior thyroid veins, which drain into the innominate or internal jugular vein.
Beginning in week 5 of gestation, 2 parathyroid glands develop from the fourth brachial pouch and 2 glands develop from the third brachial pouch, then descend to a position inferior to the fourth pouch’s glands (superior and inferior parathyroid glands, respectively).
Final parathyroid position is on the posterior aspect of the thyroid gland.
Parathyroid blood supply usually comes from the inferior thyroid artery.
The RLN lies in a triangle between the carotid artery laterally, the trachea medially, and the thyroid superiorly and typically follows the course of the inferior thyroid artery (Figure 39.1).3,4
EPIDEMIOLOGY AND ETIOLOGY
Epidemiology
Two billion people in the world are at risk for iodine deficiency-induced goiter.
Iodine supplementation has decreased the incidence of iodine-deficiency goiter in the United States, Canada, and Western Europe; however, countries in Africa still require further efforts to provide iodine supplementation.
20% of thyroid nodules in children contain cancer, higher than in adults, although the rate is decreasing owing to less common use of neck irradiation.
Risk of thyroid dysfunction is 25% in patients receiving >25 Gy of neck irradiation.
There is a risk of hyperparathyroidism and medullary thyroid cancer in multiple endocrine neoplasia subtypes.
Etiologies of Thyroid and Parathyroid Disease
Congenital hypothyroidism: inborn errors of thyroid hormone production, thyroid agenesis, maternal ingestion of antithyroid medications or goitrogens (lithium, kelp, and expectorants), transplacental passage of thyroid-blocking or stimulating antibodies, immature pituitary-thyroid axis due to prematurity, maternal iodine deficiency
Congenital hyperthyroidism: transplacental passage of thyroid-stimulating antibodies (maternal Graves disease), activating mutations in the thyroid-stimulating hormone (TSH)-receptor
Acquired hypothyroidism: iodine deficiency, Hashimoto thyroiditis, radiation exposure, liver hemangiomas, ingestion of goitrogens
Acquired hyperthyroidism: functional thyroid adenoma, subacute thyroiditis, acute suppurative thyroiditis, Graves disease, toxic goiter
Other: thyroid cyst, thyroid teratoma, thyroid carcinoma, infiltrative disease
Hyperparathyroidism: functional parathyroid adenoma or carcinoma, multiple endocrine neoplasia (MEN) types 2A and 2B, chronic kidney disease secondary to congenital or acquired renal defects, PTHrP secretion from mesoblastic nephroma, rhabdomyosarcoma, neuroblastoma
Hypoparathyroidism: DiGeorge syndrome, iatrogenic following thyroid surgery4
 Figure 39.1 Thyroid gland and neck anatomy. (Reprinted with permission from Myers E, Ferris R. Master Techniques in Otolaryngology – Head and Neck Surgery. Vol 2. Philadelphia, PA: Lippincott Williams & Wilkins; 2013.) |
CLINICAL PRESENTATION
Benign or malignant disease may present as an incidentally discovered thyroid nodule or palpable cervical lymph node on physical examination.
Frank goiter occurs secondary to thyroid overstimulation or underproduction of thyroid hormone and, based on the size, may cause obstructive symptoms such as dysphagia, hoarseness, Horner syndrome, vocal cord palsy, and breathing difficulty.
Hypothyroidism presents with galactorrhea, precocious puberty or gynecomastia in males, and classical findings of weight gain, cold intolerance, and hypoactive deep tendon reflexes.
Hyperthyroidism
Graves disease presents with nervousness, emotional lability, declining performance in school, and classical signs such as weight loss, heat intolerance, and diaphoresis; exophthalmos is uncommon.
Subacute thyroiditis presents with a tender thyroid gland after upper respiratory tract infection and with possible symptoms of thyrotoxicosis such as arrhythmias.
Acute suppurative thyroiditis presents with an erythematous and tender thyroid, systemic signs, and possible fluctuance.
Hyperparathyroidism presents with an incidental finding of elevated serum calcium or symptoms of hypercalcemia such as bone pain, nephrocalcinosis, abdominal pain, and psychiatric disturbances.
Neonatal presentation: respiratory distress, failure to thrive, and hypotonia.
DIAGNOSIS
Thyroid Disease
Neonatal screening: TSH and free T4
Low TSH and low T4 suggests secondary (central) hypothyroidism → confirmatory thyrotropin-releasing hormone stimulation test
High TSH and low T4 suggests primary hypothyroidism → measure urinary iodine excretion, test for thyroid autoantibodies, obtain thyroid ultrasound or thyroid radioiodine uptake scan to evaluate for ectopic thyroid or thyroid agenesis
Normal TSH and low T4 in premature neonates suggests immature pituitary-thyroid axis → recheck thyroid studies at 2 and 4 weeks of age
Routine thyroid hormone screening in infants, children, and adolescents → follows the same workup as described for neonates4,5,6,7
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